Component

Mouse Lrp2-null genotype

Mouse Lrp2-null genotype

2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What it acts on

  1. Kidney cortex B12 content in megalin-deficient mice was approximately fourfold lower than in controls.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Megalin-deficient versus control mice
    exposure
    Genetic megalin deficiency
    limitations
    Renal content is not a universal marker of whole-body or neural B12 sufficiency; reserve function remains an interpretation.
    nutrient_topic
    Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
    organism
    Mus musculus
    plain_language
    Impaired renal uptake depleted the kidney B12 pool in mice.
    primary_references
    [birn-2002-megalin] Megalin is essential for renal proximal tubule reabsorption and accumulation of transcobalamin-B(12). (2002). https://pubmed.ncbi.nlm.nih.gov/11832420/ DOI: 10.1152/ajprenal.00206.2000
    tissue_or_cell_type
    Kidney cortex
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 426–437

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Megalin-deficient versus control mice · source_derived_draft · unverified_draft

    ### b12-abs-megalin-kidney-store Kidney cortex B12 content in megalin-deficient mice was approximately fourfold lower than in controls. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Impaired renal uptake depleted the kidney B12 pool in mice. organism: Mus musculus tissue_or_cell_type: Kidney cortex experimental_model: Megalin-deficient versus control mice limitations: Renal content is not a universal marker of whole-body or neural B12 sufficiency; reserve function remains an interpretation. exposure: Genetic megalin deficiency cross_nutrient: false [birn-2002-megalin] Megalin is essential for renal proximal tubule reabsorption and accumulation of transcobalamin-B(12). (2002). https://pubmed.ncbi.nlm.nih.gov/11832420/ DOI: 10.1152/ajprenal.00206.2000
    Complete structured claim and evidence
  2. Megalin-deficient mice excreted approximately fourfold more urinary B12 than controls, consistent with defective renal recovery of transcobalamin-B12.

    Mouse Lrp2-null genotype → Urinary cobalamin excretion source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Megalin-deficient versus control mice
    exposure
    Genetic megalin deficiency
    limitations
    Mouse renal evidence; the fourfold urinary amount differs from the separately reported 28-fold clearance increase.
    nutrient_topic
    Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B12 (cobalamins)
    organism
    Mus musculus
    plain_language
    Without megalin, mice lost more B12 in urine.
    primary_references
    [birn-2002-megalin] Megalin is essential for renal proximal tubule reabsorption and accumulation of transcobalamin-B(12). (2002). https://pubmed.ncbi.nlm.nih.gov/11832420/ DOI: 10.1152/ajprenal.00206.2000
    tissue_or_cell_type
    Kidney proximal tubule/urine
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin B12: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 413–424

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Megalin-deficient versus control mice · source_derived_draft · unverified_draft

    ### b12-abs-megalin-urinary-loss Megalin-deficient mice excreted approximately fourfold more urinary B12 than controls, consistent with defective renal recovery of transcobalamin-B12. Condition category: machinery_impairment nutrient_topic: Vitamin B12 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Without megalin, mice lost more B12 in urine. organism: Mus musculus tissue_or_cell_type: Kidney proximal tubule/urine experimental_model: Megalin-deficient versus control mice limitations: Mouse renal evidence; the fourfold urinary amount differs from the separately reported 28-fold clearance increase. exposure: Genetic megalin deficiency cross_nutrient: false [birn-2002-megalin] Megalin is essential for renal proximal tubule reabsorption and accumulation of transcobalamin-B(12). (2002). https://pubmed.ncbi.nlm.nih.gov/11832420/ DOI: 10.1152/ajprenal.00206.2000
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards